Nerve injury-induced calcium channel alpha-2-delta-1 protein dysregulation leads to increased pre-synaptic excitatory input into deep dorsal horn neurons and neuropathic allodynia

摘要

Background: Up-regulation of voltage-gated calcium channel alpha(2)delta(1) subunit post spinal nerve ligation (SNL) injury or in alpha(2)delta(1)-overexpressing transgenic (Tg) mice correlates with tactile allodynia, a pain state mediated mainly by A beta sensory fibres forming synaptic connections with deep dorsal horn (DDH) neurons. It is not clear, however, whether dysregulated alpha(2)delta(1) alters DDH synaptic neurotransmission that underlies tactile allodynia development post nerve injury.